Neuropathology最新文献

{"title":"Increase in cathepsin K gene expression in Duchenne muscular dystrophy skeletal muscle.","authors":"Shigemi Kimura, Noriko Miyake, Shiro Ozasa, Hiroe Ueno, Yoshinobu Ohtani, Yutaka Takaoka, Ichizo Nishino","doi":"10.1111/neup.12995","DOIUrl":"10.1111/neup.12995","url":null,"abstract":"<p><p>Dystrophinopathy is caused by alterations in the dystrophin gene. The severe phenotype, Duchenne muscular dystrophy (DMD), is caused by a lack of dystrophin in skeletal muscles, resulting in necrosis and regenerating fibers, inflammatory cells, and muscle fibrosis. Progressive muscle weakness is a characteristic finding of this condition. Here, we encountered a rare case of a 10-year-old patient with asymptomatic dystrophinopathy with no dystrophin expression and investigated the reason for the absence of muscle weakness to obtain therapeutic insights for DMD. Using RNA-seq analysis, gene expression in skeletal muscles was compared among patients with asymptomatic dystrophinopathy, three patients with typical DMD, and two patients without dystrophinopathy who were leading normal daily lives. Cathepsin K (CTSK), myosin heavy chain 3 (MYH3), and nodal modulator 3-like genes exhibited a >8-fold change, whereas crystallin mu gene (CRYM) showed a <1/8-fold change in patients with typical DMD compared with their expression in the patient with asymptomatic dystrophinopathy. Additionally, CTSK and MYH3 expression exhibited a >16-fold change (P < 0.01), whereas CRYM expression showed a <1/16-fold change (P < 0.01) in patients with typical DMD compared with their expression in those without dystrophinopathy. CTSK plays an essential role in skeletal muscle loss, fibrosis, and inflammation in response to muscles injected with cardiotoxin, one of the most common reagents that induce muscle injury. Increased CTSK expression is associated with muscle injury or necrosis in patients with DMD. The lack of muscle weakness in the patient with asymptomatic dystrophinopathy might be attributed to the low CTSK expression in the muscles. To the best of our knowledge, this is the first report to demonstrate that CTSK expression was significantly higher in the skeletal muscles of patients with DMD with a typical phenotype than in those without dystrophinopathy.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"411-421"},"PeriodicalIF":1.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141627211","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Diffuse leptomeningeal glioneuronal tumor with distinct neuronal and glial components but identical diagnostic molecular and genetic features.","authors":"Andrew J Witten, Carson Dougherty, Chunhai Hao","doi":"10.1111/neup.12996","DOIUrl":"10.1111/neup.12996","url":null,"abstract":"<p><p>The 2021 World Health Organization (WHO) classification of the central nervous system (CNS) tumors has classified diffuse leptomeningeal glioneuronal tumor (DLGNT) as a mixed neuronal and glial tumor. Here, we report a DLGNT with two distinct morphological tumor components but identical molecular features. A four-year-old female child presented with progressive right upper extremity weakness. Magnetic resonance imaging (MRI) revealed the leptomeningeal enhancement over the brain stem and cervicothoracic spine. The histological examination of surgical specimens revealed two distinct tumor components: approximately half of the tumor is composed of oligodendroglioma-like tumor intermingled with nodules of ganglioglioma-like tumor. Immunohistochemistry confirmed the oligodendroglioma and ganglioglioma features. The molecular genetic studies demonstrated the features of DLGNT, including fusion of KIAA1549::BRAF, deletion of chromosome 1p, and absence of isocitrate dehydrogenase 1/2 (IDH1/2) mutation in both tumor components. Interestingly, the genetic studies also revealed the distinct chromosomal abnormalities of the loss of chromosome 4 only in oligodendroglioma-like tumor and copy neutral loss of heterozygosity of 7Q34Q36.3 in the ganglioglioma-like tumor component. This case highlights the critical role of molecular testing in the diagnosis of rare cases of DLGNT with diverse morphological components as well as in the identification of unique molecular alternations responsible for morphological phenotypes of the distinct tumors in DLGNT.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"440-444"},"PeriodicalIF":1.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11608919/pdf/","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141788738","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"OA","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Amyloid-beta pathology in a case with dementia with Lewy bodies with a rapidly progressive clinical course similar to Creutzfeldt-Jacob disease.","authors":"Shintaro Fujii, Ikuko Takahashi-Iwata, Yuki Oshima, Kazuhiro Horiuchi, Zenichi Tanei, Katsuya Satoh, Tetsuyuki Kitamoto, Shinya Tanaka, Ichiro Yabe","doi":"10.1111/neup.13017","DOIUrl":"https://doi.org/10.1111/neup.13017","url":null,"abstract":"<p><p>Most cases of dementia with Lewy bodies (DLB) follow a chronic course. However, some cases of rapidly progressive dementia (RPD) are difficult to distinguish from other diseases. Herein, we report how to differentiate DLB presenting with RPD from other diseases and its pathological features, with examples from our own experience. A 70-year-old man with RPD and psychiatric symptoms, including hallucinations and delusions, was transferred to our hospital. We suspected Creutzfeldt-Jakob disease (CJD), but disease-specific tests were all negative. The patient was treated with corticosteroids on the suspicion of an autoimmune condition; however, his symptoms did not improve. Based on the results of nuclear medicine and other tests, we suspected DLB and administered anti-Parkinsonian drugs; however, they were ineffective, and the patient died. Brain autopsy revealed extensive deposits of Lewy bodies, which were pathologically diagnosed as DLB. Additionally, extensive deposition of senile plaques was observed; however, neurofibrillary tangles (NFTs) were not prominent. DLB generally presents as a chronic disease. However, some patients with DLB present with RPD; therefore, the differential diagnosis of other diseases, such as CJD, is very important. In addition, although this case was not diagnosed with Alzheimer's disease (AD) due to the lack of NFTs, extensive amyloid deposition was observed in the brain tissue. Previous reports have described cases of RPD with amyloid deposition alone, and in this case too, it is suggested that amyloid deposition might have had a strong influence on the clinical course of RPD.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142770709","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Elevated expression of N-myc downstream regulated gene 1 protein in glioblastomas reflects tumor angiogenesis and poor patient prognosis.","authors":"Yasuo Sugita, Takuya Furuta, Kenji Takahashi, Koichi Higaki, Yuichi Murakami, Michihiko Kuwano, Mayumi Ono, Hideyuki Abe, Jun Akiba, Motohiro Morioka","doi":"10.1111/neup.12999","DOIUrl":"10.1111/neup.12999","url":null,"abstract":"<p><p>N-myc downstream regulated gene 1 (NDRG1) is a member of the NDRG family, of which four members (NDRG1, NDRG2, NDRG3, and NDRG4) have been identified. NDRG1 is repressed by c-MYC and N-MYC proto-oncogenes. NDRG1 is translated into a 43 kDa protein that is associated with the regulation of cellular stress responses, proliferation, and differentiation. In this study, we aimed to clarify the relationship between progression of glioblastoma (GB) IDH-wildtype and NDRG1 expression in tumor cells. We assessed the expression of NDRG1 in 41 GBs using immunostaining and evaluated its prognostic significance. NDRG1 expression by GBs was evaluated using Histoscore, which showed high and low scores in 23 and 18 cases, respectively. NDRG1-positive cells were strongly expressed in Ki-67 labeled proliferating tumor cells and CD105 positive proliferating microvessels around the area of palisading necrosis. Statistical analyses showed lower survival rates in the high-score group than the low-score group (P < 0.01). This study indicated that overexpression of NDRG1 by GB reflects tumor angiogenesis and poor patient prognosis.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"422-431"},"PeriodicalIF":1.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893977","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Ipsilateral simultaneous multiple hypertensive intracerebral hemorrhages: Analysis of hematoma formation and comparison with distribution of hypertensive mixed-type hematoma.","authors":"Shigeki Takeda, Hitoshi Takahashi, Teruo Miyakawa, Kazunori Yamazaki, Kiyoshi Onda","doi":"10.1111/neup.12998","DOIUrl":"10.1111/neup.12998","url":null,"abstract":"<p><p>A 55-year-old Japanese woman with a history of hypertension and right putaminal hemorrhage developed simultaneous hemorrhages in the left thalamus and putamen and died 24 h later. There were no vascular anomalies in the brain. Synaptophysin immunostaining combined with eosin azure 50 (EA50) staining clearly identified the hematoma and the surrounding brain structures. In the right cerebral hemisphere, a cystic lesion as a sequela of the usual type of hypertensive putaminal hematoma was evident. In the left cerebral hemisphere, two fresh hematomas were evident. One was a thalamic hematoma, which had destroyed the dorsal and medial structures of the thalamus, and the other was an unusual putaminal hematoma, which had destroyed the entire putamen and crossed the internal capsule and caudate nucleus. α-Smooth muscle actin immunostaining combined with EA50 and Victoria bleu staining demonstrated three ruptured arteries associated with fibrin aggregates in the anterior thalamic nucleus and anterior putamen. Some circular structures composed of fibrin, suggesting the presence of ruptured arteries in the neighborhood, were evident in the thalamus and putamen. In the putamen, ruptured arteries and circular structures were present in the lateral to medial areas. Fibrin aggregates in the anterior thalamic nucleus were more numerous than those in the putamen. On the basis of these findings, we concluded that: (i) the artery with numerous fibrin aggregates in the anterior thalamic nucleus had ruptured first, followed by the arteries distributed in other parts of the thalamus and putamen; (ii) the unusual putaminal hematoma was attributable to rupture of the arteries around the center of the putamen, which are not responsible for the usual type of hypertensive putaminal hematoma; and (iii) it is suggested that even if hypertensive hemorrhage occurs simultaneously in the ipsilateral putamen and thalamus, the usual type of hypertensive mixed-type hematoma does not form.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"445-451"},"PeriodicalIF":1.3,"publicationDate":"2024-12-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"141893921","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Morphometry of choroid plexus epithelial cells in neurodegenerative diseases.","authors":"Ryuta Murakami, Yoichi Chiba, Nobuyuki Miyatake, Yumi Miyai, Koichi Matsumoto, Keiji Wakamatsu, Yuko Saito, Manato Hara, Shigeo Murayama, Masaki Ueno","doi":"10.1111/neup.13019","DOIUrl":"https://doi.org/10.1111/neup.13019","url":null,"abstract":"<p><p>The choroid plexus not only secretes the majority of cerebrospinal fluid but also controls the circadian rhythm, which can be impaired in the presence of neurodegenerative diseases. In addition, many studies have reported the contribution of choroid plexus abnormalities to the pathogenesis of neurodegenerative diseases, including Alzheimer's disease (AD). Formalin-fixed paraffin-embedded blocks were obtained from the lateral ventricles of the brains of four subjects with AD, four with vascular dementia, four with Parkinson's disease, three with multiple system atrophy, and five control patients with unremarkable neuropathological findings. They were sectioned and routinely stained with hematoxylin and eosin. Morphological analysis of epithelial cells in 10 high-power fields or a total area per case was conducted using digital images. There were no significant changes in any of the measurements: epithelial cell area, long and short axes, and ratio of the epithelial cell area to total stained area among the five groups. However, a simple linear regression analysis of epithelial cells in 20 patients showed that age was significantly correlated with the cell area, long axis, and short axis but not ratio. There were no effects of hypertension, diabetes mellitus, or calcification in the stroma on the measurements. These findings indicate that age was associated with the cell area and size in choroid plexus epithelial cells, whereas no significant changes in any epithelial cell measurements were present in neurodegenerative diseases.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-27","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142739958","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"A glioneuronal tumor with neurocytic rosettes harboring FGFR1 internal tandem duplication - A report of a unique case.","authors":"Jiri Soukup, Nikola Hajkova, Veronika Hajkova, Marian Svajdler, David Netuka, Martin Majovsky","doi":"10.1111/neup.13018","DOIUrl":"https://doi.org/10.1111/neup.13018","url":null,"abstract":"<p><p>Rosette-forming glioneuronal tumors (RGNTs) with FGFR1 tyrosine kinase domain internal tandem duplication (FGFR1 ITD) is exceedingly rare, with only a few cases reported in the literature. Hereby we present a case of a tumor with RGNT morphology occurring in area of septum pellucidum of 43-year-old male. The tumor showed FGFR1 ITD, no PIK3CA, PIK3R1 or NF1 alterations and inconclusive methylation profile with match for class of \"low-grade glial/glioneuronal/neuroepithelial tumors\". No areas characteristic of dysembryoplastic neuroepithelial tumor were identified. A brief review of literature on discrepancies between morphological diagnosis of RGNT and molecular profile of the entity is provided.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142716666","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"MYB::QKI fusion-positive diffuse glioma of the cerebellum: A case report.","authors":"Kaishi Satomi, Takahiro Shibayama, Takashi Hibiya, Akimasa Hayashi, Kiyotaka Nagahama, Kenichiro Kato, Yukino Nikai, Yuko Matsushita, Miho Gomyo, Yuki Yamagishi, Nobuyoshi Sasaki, Kuniaki Saito, Keiichi Kobayashi, Anna Takeda, So Fujimoto, Takeshi Matsuo, Keisuke Takai, Takashi Komori, Kazuhiro Tsuchiya, Motoo Nagane, Koichi Ichimura, Junji Shibahara","doi":"10.1111/neup.13016","DOIUrl":"https://doi.org/10.1111/neup.13016","url":null,"abstract":"<p><p>Angiocentric glioma (AG) is a supratentorial diffuse low-grade glioma characterized by the MYB::QKI fusion gene, showing angiocentric growth of monomorphous spindle cells with astrocytic and ependymal immunophenotypes. We describe a rare case of MYB::QKI fusion-positive diffuse cerebellar glioma in a 54-year-old male. The patient initially presented with a T2/FLAIR hyperintense lesion in the left cerebellar hemisphere and slowly progressive neurological symptoms. Histopathological evaluation revealed a diffuse glioma characterized by spindle-shaped and small epithelioid cells with perivascular infiltration. Immunohistochemistry showed positivity for glial fibrillary acidic protein and only occasionally positive for Olig2. No dot- or ring-like epithelial membrane antigen immunoreactivity was observed. In this case, the proliferative activity was higher than that in typical AG cases, as manifested by multiple mitoses (four mitoses/slide) and a Ki-67 labeling index of 5%. The tumor cells were negative for IDH1 p.R132H and H3 p.K28M mutation-specific antibodies. Fluorescence in situ hybridization showed a MYB break-apart signal, and reverse transcription-polymerase chain reaction analysis confirmed an in-frame MYB (6q23.3, exon 11, NM_001161659.2)::QKI (6q26, exon 5, NM_006775.3) fusion. IDH1 p.R132, IDH2 p.R172, H3-3A p.K28, H3C2 p.K28, and BRAF p.V600 were all wild type. DNA methylome profiling did not match any of the established methylation classes, including the four subtypes of diffuse glioma, MYB- or MYBL1-altered. Considering the results of DNA methylome profiling, the question remains as to whether this case represents a subset of AG (diffuse glioma, MYB/MYBL1-altered) or a distinct subtype. Although the morphological findings and the presence of fusion indicated that the tumor was a cerebellar AG, the DNA methylome profile did not match that of AG. An accumulation of more cases is needed to determine the precise nature of the tumor, which may lead to an expansion of the tumor concept.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142682248","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"Utilizing quantitative susceptibility mapping to differentiate primary lateral sclerosis from progressive supranuclear palsy: A case report.","authors":"Hiroaki Sekiya, Ryota Satoh, Farwa Ali, Dennis W Dickson, Jennifer L Whitwell, Keith A Josephs","doi":"10.1111/neup.13015","DOIUrl":"10.1111/neup.13015","url":null,"abstract":"<p><p>We report a patient who presented clinically with progressive supranuclear palsy (PSP) but was pathologically diagnosed as having primary lateral sclerosis (PLS) with magnetic resonance imaging (MRI) with a quantitative susceptibility mapping (QSM) protocol. A 70-year-old man was clinically diagnosed with PSP due to early falls and unresponsiveness to levodopa therapy. Postmortem pathological examination revealed mild loss of Betz cells, gliosis, and transactive response DNA binding protein of 43 kDa (TDP-43)-positive inclusions in the motor cortex, leading to the pathological diagnosis of PLS. To explore methods for differentiating PLS from PSP, ante-mortem QSM images were visually and quantitatively assessed for abnormal increases in magnetic susceptibility in the motor cortex. Prussian blue and Luxol fast blue combined with periodic acid-Schiff staining were also performed to understand the source of the susceptibility increases. QSM showed clear hyperintense signals in the motor cortex. Magnetic susceptibility in the motor cortex was higher in the PLS patient (Z = 4.7, p < 0.001) compared to normal controls and pathologically diagnosed PSP patients. Pathological examination of the region showed intracortical myelin loss, as well as iron deposition. Underlying pathological processes for the increased magnetic susceptibility include not only iron deposition but also intracortical myelin. Our case suggests that QSM is a potential tool to differentiate PLS from PSP, providing insights for accurate diagnosis and enhancing clinical decision-making.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":""},"PeriodicalIF":1.3,"publicationDate":"2024-11-18","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142668626","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}

{"title":"In-house molecular diagnosis of diffuse glioma updating the revised WHO classification by a platform of the advanced medical care system, Senshin-Iryo.","authors":"Nobuhiro Hata, Yutaka Fujioka, Ryosuke Otsuji, Daisuke Kuga, Ryusuke Hatae, Yuhei Sangatsuda, Takeo Amemiya, Naoki Noguchi, Aki Sako, Minoru Fujiki, Masahiro Mizoguchi, Koji Yoshimoto","doi":"10.1111/neup.12970","DOIUrl":"10.1111/neup.12970","url":null,"abstract":"<p><p>Since the World Health Organization (WHO) 2016 revision, the number of molecular markers required for diffuse gliomas has increased, placing a burden on clinical practice. We have established an in-house, molecular diagnostic platform using Senshin-Iryo, a feature of Japan's unique healthcare system, and partially modified the analysis method in accordance with the WHO 2021 revision. Herein, we review over a total 5 years of achievements using this platform. Analyses of IDH, BRAF, and H3 point mutations, loss of heterozygosity (LOH) on 1p/19q and chromosomes 10 and 17, and MGMT methylation were combined into a set that was submitted to Senshin-Iryo as \"Drug resistance gene testing for anticancer chemotherapy\" and was approved in August 2018. Subsequently, in October 2021, Sanger sequencing for the TERT promoter mutation was added to the set, and LOH analysis was replaced with multiplex ligation-dependent probe amplification (MLPA) to analyze 1p/19q codeletion and newly required genetic markers, such as EGFR, PTEN, and CDKN2A from WHO 2021. Among the over 200 cases included, 54 were analyzed after the WHO 2021 revision. The laboratory has maintained a diagnostic platform where molecular diagnoses are confirmed within 2 weeks. Initial expenditures exceeded the income from patient copayments; however, it has gradually been reduced to running costs alone and is approaching profitability. After the WHO 2021 revision, diagnoses were confirmed using molecular markers obtained from Senshin-Iryo in 38 of 54 cases (70.1%). Among the remaining 16 patients, only four (7.4%) were diagnosed with diffuse glioma, not elsewhere classified, which was excluded in 12 cases where glioblastoma was confirmed by histopathological diagnosis. Our Senshin-Iryo trial functioned as a salvage system to overcome the transition period between continued revisions of WHO classification that has caused a clinical dilemma in the Japanese healthcare system.</p>","PeriodicalId":19204,"journal":{"name":"Neuropathology","volume":" ","pages":"344-350"},"PeriodicalIF":1.3,"publicationDate":"2024-10-01","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"140110897","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}